REM sleep is characterized by "paradoxical" changes in motor function. CNS structures that depolarize motoneurons show activity levels exceeding those of active waking, while simultaneous motoneuron hyperpolarization blocks motor output. Pathological activity in the systems responsible for motor inhibition and motor activation in REM sleep is believed to cause cataplexy, the sudden loss of muscle tone experienced by narcoleptics and the REM sleep behavior disorder. The loss of tone in accessory respiratory muscles during REM sleep causes the most severe oxygen desaturations of sleep apnea. The mechanisms responsible for these motor changes are poorly understood. We have found that electrical stimulation of the nucleus magnocellularis (NMC) of the medial medulla with a single pulse train causes a complete suppression of muscle tone. Repetitive stimulation produces locomotor movements. We demonstrated that the muscle tone suppression from NMC is triggered by non-NMDA glutamate receptors while the locomotion is triggered by NMDA receptors. The activation of both NMDA and non-NMDA receptors in NMC by glutamate release can explain the combination of atonia and motor activation that characterizes REM sleep. We found that lesions of NMC block the atonia of REM sleep. In studies of the narcoleptic dog, we found that a subpopulation of NMC neurons is active only during cataplexy and REM sleep. The goal of the present study is to analyze the NMC motor system. We hypothesize that locomotion and atonia are mediated by two distinct groups of glutamate sensitive neurons within NMC. We will test this hypothesis by extracellular unit recording and spike triggered averaging of muscle activity. We will characterize the inputs, morphology and transmitter of NMC atonia active cells using intracellular recording, intracellular staining and iontophoresis. We will map and contrast the properties of cell populations active during atonia with those active during locomotion, using c-fos immunohistochemistry. We will determine the distribution of non-NMDA receptors on each cell type, using an antibody to the AMPA receptor. This work will lead to a better understanding of the mechanism producing muscle atonia and motor activation in REM sleep. It will clarify the means by which this mechanism might be disturbed in narcolepsy, the REM behavior disorder, sleep apnea and other disorders of muscle tone control.